We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Papers
61,005 resultsShowing papers similar to Polystyrene microplastics cause cardiac fibrosis by activating Wnt/β-catenin signaling pathway and promoting cardiomyocyte apoptosis in rats
ClearThe impact of polystyrene microplastics on cardiomyocytes pyroptosis through NLRP3/Caspase‐1 signaling pathway and oxidative stress in Wistar rats
Researchers exposed rats to polystyrene microplastics at varying doses and examined the effects on heart tissue. They found that microplastic exposure triggered inflammatory cell death and oxidative stress in heart cells through a specific signaling pathway, suggesting that microplastics may pose risks to cardiovascular health.
Polystyrene microplastics induce myocardial inflammation and cell death via the TLR4/NF-κB pathway in carp
Researchers exposed carp to polystyrene microplastics and found they caused heart tissue inflammation, cell death, and necrosis through activation of the TLR4/NF-kB inflammatory pathway. The damage increased with higher microplastic concentrations, with both apoptosis and necrosis observed in heart muscle cells. The study provides evidence that microplastic exposure can directly harm cardiovascular tissue in fish.
Dissection of the potential mechanism of polystyrene microplastic exposure on cardiomyocytes
Researchers investigated how polystyrene microplastics affect human heart muscle cells at concentrations reflecting estimated daily human intake levels. They found that the microplastics caused oxidative stress, mitochondrial dysfunction, and disrupted calcium signaling in the cells. The study suggests that microplastic exposure may contribute to cardiovascular risks by directly damaging heart cell function at the cellular level.
Cardiotoxicity of polystyrene nanoplastics and associated mechanism of myocardial cell injury in mice
Mice exposed to polystyrene nanoplastics for 42 days developed enlarged hearts, thinner heart walls, and weaker heart contractions in a dose-dependent manner. The nanoplastics triggered inflammation and oxidative stress in heart muscle cells through specific signaling pathways. These findings suggest that nanoplastic exposure could contribute to heart disease, including a condition called dilated cardiomyopathy.
Polystyrene nanoplastics exacerbate lipopolysaccharide-induced myocardial fibrosis and autophagy in mice via ROS/TGF-β1/Smad
Researchers found that polystyrene nanoplastics worsened heart damage in mice already exposed to bacterial toxins, accelerating scarring and disrupting normal heart tissue maintenance. The combined exposure triggered increased oxidative stress and activated a specific signaling pathway linked to tissue fibrosis. The study suggests that nanoplastic exposure could amplify existing cardiac stress, potentially compounding heart problems when the body is already under inflammatory challenge.
Intratracheal administration of polystyrene microplastics induces pulmonary fibrosis by activating oxidative stress and Wnt/β-catenin signaling pathway in mice
Researchers administered polystyrene microplastics directly into the lungs of mice and found that the particles induced pulmonary fibrosis by triggering oxidative stress and activating the Wnt signaling pathway. The microplastics caused damage to the lung lining cells and promoted the buildup of scar tissue in lung tissue. The study provides evidence that inhaled microplastics may contribute to serious respiratory conditions by driving fibrotic changes in the lungs.
Polystyrene nanoplastics induce cardiotoxicity by upregulating HIPK2 and activating the P53 and TGF-β1/Smad3 pathways
Researchers demonstrated that oral exposure to polystyrene nanoplastics in mice causes cardiac fibrosis, cardiomyocyte death, and impaired heart function by upregulating the protein HIPK2 and activating P53 and TGF-β1/Smad3 signaling pathways, with effects worsened in animals with pre-existing heart disease — implicating nanoplastics as a cardiovascular risk factor.
Low-dose of polystyrene microplastics induce cardiotoxicity in mice and human-originated cardiac organoids
Researchers found that even low doses of polystyrene microplastics can damage heart tissue in both mice and lab-grown human heart organoids. The microplastics triggered oxidative stress and disrupted energy production in heart cells, leading to inflammation and cell death. This is one of the first studies to show heart-specific toxicity from microplastics at doses meant to reflect realistic human exposure levels.
Polystyrene microplastics-induced cardiotoxicity in chickens via the ROS-driven NF-κB-NLRP3-GSDMD and AMPK-PGC-1α axes
Researchers found that polystyrene microplastics caused serious heart damage in chickens by triggering oxidative stress, inflammation, and disruption of the cells' energy production systems. The microplastics activated inflammatory pathways that led to a type of cell death called pyroptosis and damaged the mitochondria that power heart cells. These findings suggest that microplastic exposure could pose risks to cardiovascular health in animals, with potential implications for understanding heart-related effects in humans.
Polystyrene nanoplastics exert cardiotoxicity through the Notch and Wnt pathways in zebrafish (Danio rerio)
Researchers exposed zebrafish embryos to polystyrene nanoplastics and found dose-dependent cardiac developmental defects linked to disruption of the Notch and Wnt signaling pathways — key regulators of heart development — alongside oxidative stress, endoplasmic reticulum stress, and reduced mitochondrial activity.
Exposure to polystyrene microplastics with different functional groups: Implications for blood pressure and heart
In a rat study, exposure to polystyrene microplastics raised blood pressure by 22-40% and caused heart muscle enlargement and oxidative damage, with chemically modified microplastics causing even worse effects. The research identified a molecular pathway involving reduced blood vessel-relaxing signals that may explain how microplastic exposure contributes to cardiovascular disease.
The cardiovascular toxicity of polystyrene microplastics in rats: based on untargeted metabolomics analysis
A rat study using metabolomics analysis found that long-term exposure to high concentrations of polystyrene microplastics led to abnormal fat metabolism and cardiovascular damage. The harm appeared to be driven by oxidative stress and inflammation, suggesting that chronic microplastic exposure could contribute to heart and blood vessel disease.
Toxicity of long term exposure to low dose polystyrene microplastics and nanoplastics in human iPSC-derived cardiomyocytes
Researchers exposed human heart cells grown from stem cells to very low doses of polystyrene micro- and nanoplastics over an extended period and found that the particles reduced the cells' ability to contract and disrupted their electrical signaling. The smaller nanoplastics (50 nm) caused more severe damage than the larger microplastics (1 micrometer), including increased cell death and calcium handling problems. This study provides direct evidence that even low-level microplastic exposure could harm human heart function.
Mechanism of Nano‐Microplastics Exposure‐Induced Myocardial Fibrosis: DKK3‐Mediated Mitophagy Dysfunction and Pyroptosis
Researchers investigated how nano-microplastic exposure leads to heart tissue scarring in mice and identified a specific molecular pathway involved. They found that the plastic particles suppressed a protein called DKK3, which disrupted the cell's ability to recycle damaged mitochondria, triggering an inflammatory cell death process that promotes fibrosis. The study reveals a potential mechanism by which long-term microplastic exposure could contribute to cardiac damage.
Exposure of polystyrene nanoplastics led to ferroptosis on cardiomyocytes
Researchers exposed rat heart cells to 100-nanometer polystyrene nanoparticles and found that the particles were taken up by the cells and triggered a form of iron-dependent cell death called ferroptosis. The nanoparticles caused a buildup of reactive oxygen species in mitochondria, iron accumulation, and damage to cell membranes. The study suggests that nanoplastic exposure may pose risks to heart health through this specific cell death pathway.
Polystyrene nanoplastics induced cardiomyocyte apoptosis and myocardial inflammation in carp by promoting ROS production
Researchers exposed carp to polystyrene nanoplastics of different sizes and found that the particles caused heart muscle cell death and cardiac inflammation. Smaller nanoplastics penetrated deeper into heart tissue and caused more severe damage by promoting the production of reactive oxygen species. The study provides evidence that nanoplastic pollution in aquatic environments can directly harm fish cardiovascular health.
Endoplasmic reticulum stress-controlled autophagic pathway promotes polystyrene microplastics-induced myocardial dysplasia in birds
Researchers exposed chicks to different concentrations of polystyrene microplastics to study their effects on heart development. The study found that microplastics triggered endoplasmic reticulum stress and disrupted autophagy pathways in cardiac tissue, leading to myocardial dysplasia in exposed birds.
Exposure to Polypropylene Microplastics Causes Cardiomyocyte Apoptosis Through Oxidative Stress and Activation of the MAPK‐Nrf2 Signaling Pathway
Researchers found that polypropylene microplastics caused heart muscle cell death in both mice and lab-grown cells by triggering oxidative stress and activating specific cell damage pathways. Mice exposed to higher concentrations showed visible heart tissue damage and inflammation. This study is one of the first to demonstrate that microplastic exposure can directly harm the heart, raising concerns about cardiovascular effects in people exposed to microplastics.
Intratracheal Administration of Polystyrene Micro(nano)plastics with a Mixed Particle Size Promote Pulmonary Fibrosis in Rats by Activating TGF-β1 Signaling and Destabilizing Mitochondrial Dynamics and Mitophagy in a Dose- and Time-Dependent Manner.
SD rats exposed to mixed polystyrene micro(nano)plastics via intratracheal administration at escalating doses over time developed pulmonary fibrosis and mitochondrial dysfunction, with severity linked to dose. The findings demonstrated a clear biological pathway connecting inhaled microplastic exposure to lung injury.
Polystyrene microplastics cause granulosa cells apoptosis and fibrosis in ovary through oxidative stress in rats
Researchers exposed female rats to polystyrene microplastics at different concentrations for 90 days and examined the effects on their ovaries. The study found that microplastic exposure caused cell death and tissue scarring in the ovaries through oxidative stress, suggesting that microplastics may have implications for female reproductive health.
Ferroptosis involved in inhaled polystyrene microplastics leaded myocardial fibrosis through HIF-ROS-SLC7A11/GPX4 Pathway
Researchers found that inhaling polystyrene microplastics caused heart muscle scarring (fibrosis) in mice through a process called ferroptosis, a type of iron-dependent cell death. The microplastics triggered a chain reaction involving low oxygen signals and oxidative stress that depleted the heart cells' protective antioxidant systems. This study reveals a specific mechanism by which breathing in airborne microplastics could lead to lasting heart damage.
Polystyrene nanoplastics trigger mitochondrial and metabolic reprogramming in cardiomyocytes: Evidence from integrated transcriptomic and metabolomic analysis
Scientists found that tiny plastic particles called nanoplastics can damage heart cells by disrupting their powerhouses (mitochondria) and reducing their ability to produce energy. When researchers exposed human heart cells and mice to these nanoplastics, they observed weakened heart function and signs of early heart damage. This research suggests that the growing amount of microscopic plastic pollution in our environment could pose previously unknown risks to heart health.
Evaluation of Polystyrene Nanoplastics Induced Cardiotoxicity Under Different Dietary Patterns in Mice
Researchers exposed mice fed different dietary patterns to polystyrene nanoplastics and assessed cardiac toxicity. The study found that dietary habits significantly modulated nanoplastic-induced heart damage, demonstrating that diet is an important variable in evaluating the health risks of foodborne plastic contaminants.
Adolescent exposure to polylactic acid microplastics causes cardiac fibrosis by promoting cardiomyocyte senescence
Adolescent mice exposed to polylactic acid (PLA) biodegradable microplastics developed cardiac fibrosis, with mechanistic studies showing that PLA particles promoted cardiomyocyte senescence and activated inflammatory signaling, demonstrating cardiotoxicity from a supposedly 'green' plastic.